tbuckley/cabot-search huggingface dataset:
Inpatient EHR User Experience and Hospital EHR Safety Performance
Authors: David C. Classen, Christopher A. Longhurst, Taylor Davis, Julia Adler Milstein, David W. Bates
Journal: JAMA Network Open (2023)

IMPORTANCE Despite the broad adoption and optimization of electronic health record (EHR) systems across the continuum of care, serious usability and safety problems persist. OBJECTIVE To assess whether EHR safety performance is associated with EHR frontline user experience in a national sample of hospitals. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study included all US adult hospitals that used the National Quality Forum Leapfrog Health IT Safety Measure and also used the ARCH Collaborative EHR User experience survey from January 1, 2017, to January 1, 2019. Data analysis was performed from September 2020 to November 2022. MAIN OUTCOMES AND MEASURES The primary outcomes were hospital performance on the Leapfrog Health IT Safety measure (overall and 10 subcomponents) and the ARCH collaborative frontline user experience scores (overall and 8 subcomponents). Ordinary least squares models with survey responses clustered by hospital were used to assess associations between the overall measures and their subcomponents. RESULTS There were 112 hospitals and 5689 frontline user surveys included in the study. Hospitals scored a mean of 0.673 (range, 0.297-0.973) on the Leapfrog Health IT safety measure; the mean ARCH EHR user experience score was 3.377 (range, 1 [best] to 5 [worst]). The adjusted β coefficient between the overall safety score and overall user experience score was 0.011 (95% CI, 0.006-0.016). The ARCH overall score was also significantly associated with 10 subcategory scores of the Leapfrog Health IT safety score, and the overall Leapfrog score was associated with the 8 subcategory scores of the ARCH user experience score. CONCLUSIONS AND RELEVANCE This cross-sectional study found a positive association between frontline user–rated EHR usability and EHR safety performance. This finding suggests that improving EHR usability, which is a current well-known pain point for EHR users, could have direct benefits in terms of improved EHR safety.
Optimizing Dosing of Trastuzumab Deruxtecan in <i>HER2</i>-Mutant Non–Small-Cell Lung Cancer: A Reminder That More Is Not Always Better
Authors: Hui Jing Hoe, Benjamin J. Solomon
Journal: Journal of Clinical Oncology (2023)

and toxicity for patients with previously treated HER2 mutation-positive NSCLC.Ongoing studies are evaluating T-DXd 5.4 mg/kg once every 3 weeks compared with chemotherapy plus pembrolizumab in the first-line setting for HER2-mutant NSCLC (DESTINY-Lung04) and in combination strategies with immunotherapy and chemotherapy.In these settings, dose optimization and mitigation of toxicities including drug-induced ILD/pneumonitis and other cumulative low-grade toxicities that are impactful for patients will be essential to enable long-term delivery of this effective new class of therapeutics and maximize therapeutic outcomes.
Tractable limitations of current polygenic scores do not excuse genetically confounded social science
Authors: Damien Morris, Stuart J. Ritchie, Alexander I. Young
Journal: Behavioral and Brain Sciences (2023)

Abstract Burt's critique of using polygenic scores in social science conflates the “scientific costs” of sociogenomics with “sociopolitical and ethical” concerns. Furthermore, she paradoxically enlists recent advances in controlling for environmental confounding to argue such confounding is scientifically “intractable.” Disinterested social scientists should support ongoing efforts to improve this technology rather than obstructing progress and excusing genetically confounded research.
Building causal knowledge in behavior genetics without racial/ethnic diversity will result in weak causal knowledge
Authors: Moin Syed
Journal: Behavioral and Brain Sciences (2023)

Abstract Behavior genetics often emphasizes methods over the underlying quality of the psychological information to which the methods are applied. A core aspect of this quality is the demographic diversity of the samples. Building causal genetic models based only on European-ancestry samples compromises their generalizability. Behavior genetics researchers must spend additional time and resources diversifying their samples before emphasizing causation.
Genome-wide association study and the randomized controlled trial: A false equivalence
Authors: Paul Siegel
Journal: Behavioral and Brain Sciences (2023)

Abstract Madole &amp; Harden's assertion that the effects derived from within-family genome-wide association studies (GWASs) and from randomized controlled trials (RCTs) are equivalent is misleading. GWASs are substantially more “non-unitary, non-uniform, and non-explanatory” than RCTs. While the within-family GWAS bring us closer to identifying genetic causes, whether it will change behavioral genetics into a causal science is an open question.
Differences in liver and mortality outcomes of non-alcoholic fatty liver disease by race and ethnicity: A longitudinal real-world study
Authors: Vy H. Nguyen, Isaac Le, Audrey Ha, Richard Hieu Le, Nicholas Ajit Rouillard, Ashley Fong, Surya Gudapati, Jung Eun Park, Mayumi Maeda, Scott Barnett, Ramsey Cheung, Mindie H. Nguyen
Journal: Clinical and Molecular Hepatology (2023)

Understanding of nonalcoholic fatty liver disease (NAFLD) continues to expand, but the relationship between race and ethnicity and NAFLD outside the use of cross-sectional data is lacking. Using longitudinal data, we investigated the role of race and ethnicity in adverse outcomes in NAFLD patients.
Ecological Momentary Assessment and Machine Learning for Predicting Suicidal Ideation Among Sexual and Gender Minority Individuals
Authors: Chang Lei, Diyang Qu, Kunxu Liu, Runsen Chen
Journal: JAMA Network Open (2023)

Suicidality poses a serious global health concern, particularly in the sexual and gender minority population. While various studies have focused on investigating chronic stressors, the precise prediction effect of daily experiences on suicide ideation remains uncertain.
Efficacy and Tolerability of Gefapixant for Treatment of Refractory or Unexplained Chronic Cough
Authors: Elena Kum, Matthew Patel, Nermin Diab, Mustafaa Wahab, Dena Zeraatkar, Derek K. Chu, Paul M. O’Byrne, Gordon H. Guyatt, Imran Satia
Journal: JAMA (2023)

Importance Gefapixant represents an emerging therapy for patients with refractory or unexplained chronic cough. Objective To evaluate the efficacy and tolerability of gefapixant for the treatment of adults with refractory or unexplained chronic cough. Data Sources MEDLINE, Embase, Cochrane Central Register of Controlled Trials, and Web of Science from November 2014 to July 2023. Study Selection Two reviewers independently screened for parallel and crossover randomized clinical trials (RCTs) that compared, in patients with refractory or unexplained chronic cough, either gefapixant with placebo, or 2 or more doses of gefapixant with or without placebo. Data Extraction and Synthesis Two reviewers independently extracted data. A frequentist random-effects dose-response meta-analysis or pairwise meta-analysis was used for each outcome. The GRADE (Grading of Recommendations, Assessment, Development, and Evaluation) approach was used to rate the certainty in whether patients would perceive the effects as important (greater than the minimal important difference [MID]) or small (less than the MID). Main Outcomes and Measures Cough frequency (measured using the VitaloJAK cough monitor; MID, 20%), cough severity (measured using the 100-mm visual analog scale [VAS]; higher score is worse; MID, 30 mm), cough-specific quality of life (measured using the Leicester Cough Questionnaire [LCQ]; score range, 3 [maximal impairment] to 21 [no impairment]; MID, 1.3 points), treatment-related adverse events, adverse events leading to discontinuation, and taste-related adverse events. Results Nine RCTs including 2980 patients were included in the primary analysis. Compared with placebo, gefapixant (45 mg twice daily) had small effects on awake cough frequency (17.6% reduction [95% CI, 10.6%-24.0%], moderate certainty), cough severity on the 100-mm VAS (mean difference, −6.2 mm [95% CI, −4.1 to −8.4]; high certainty), and cough-specific quality of life on the LCQ (mean difference, 1.0 points [95% CI, 0.7-1.4]; moderate certainty). Compared with placebo, gefapixant (45 mg twice daily) probably caused an important increase in treatment-related adverse events (32 more per 100 patients [95% CI, 13-64 more], moderate certainty) and taste-related adverse events (32 more per 100 patients [95% CI, 22-46 more], high certainty). High-certainty evidence suggests that gefapixant (15 mg twice daily) had small effects on taste-related adverse events (6 more per 100 patients [95% CI, 5-8 more]). Conclusions and Relevance Compared with placebo, gefapixant (45 mg orally twice daily) led to modest improvements in cough frequency, cough severity, and cough-specific quality of life but increased taste-related adverse events.
Causal complexity in human research: On the shared challenges of behavior genetics, medical genetics, and environmentally oriented social science
Authors: James W. Madole, K. Paige Harden
Journal: Behavioral and Brain Sciences (2023)

Abstract We received 23 spirited commentaries on our target article from across the disciplines of philosophy, economics, evolutionary genetics, molecular biology, criminology, epidemiology, and law. We organize our reply around three overarching questions: (1) What is a cause? (2) How are randomized controlled trials (RCTs) and within-family genome-wide association studies (GWASs) alike and unalike? (3) Is behavior genetics a qualitatively different enterprise? Throughout our discussion of these questions, we advocate for the idea that behavior genetics shares many of the same pitfalls and promises as environmentally oriented research, medical genetics, and other arenas of the social and behavioral sciences.
Meeting counterfactual causality criteria is not the problem
Authors: Kristian E. Markon
Journal: Behavioral and Brain Sciences (2023)

Abstract Counterfactual causal interpretations of family genetic effects are appropriate, but neglect an important feature: Provision of unique information about expected outcomes following an independent decision, such as a decision to intervene. Counterfactual causality criteria are unlikely to resolve controversies about behavioral genetic findings; such controversies are likely to continue until counterfactual inferences are translated into interventional hypotheses and designs.
Where <i>not</i> to look for targets of social reforms and interventions, according to behavioral genetics
Authors: Nikolai Haahjem Eftedal, Lotte Thomsen
Journal: Behavioral and Brain Sciences (2023)

Behavioral genetics typically finds that the so-called shared environment contributes little or nothing to explaining within-population variation on most traits. If true, this has important implications for where not to look for good targets of interventions: Namely all things that are within the normal range of variation from one rearing environment to the next in that population.
A disanalogy with RCTs and its implications for second-generation causal knowledge
Authors: Kate E. Lynch, Rachael L. Brown, Jeremy Strasser, Shang Long Yeo
Journal: Behavioral and Brain Sciences (2023)

Abstract We are less optimistic than Madole &amp; Harden that family-based genome-wide association studies (GWASs) will lead to significant second-generation causal knowledge. Despite bearing some similarities, family-based GWASs and randomised controlled trials (RCTs) are not identical. Most RCTs assess a relatively homogenous causal stimulus as a treatment, whereas GWASs assess highly heterogeneous causal stimuli. Thus, GWAS results will not translate so easily into second-generation causal knowledge.
Ambient fine particulate matter and breast cancer incidence in a large prospective US cohort
Authors: Alexandra J White, Jared A Fisher, Marina R Sweeney, Neal D Freedman, Joel D Kaufman, Debra T Silverman, Rena R Jones
Journal: JNCI Journal of the National Cancer Institute (2023)

Abstract Background Fine particulate matter (PM2.5) has been inconsistently associated with breast cancer incidence, however, few studies have considered historic exposure when levels were higher. Methods Outdoor residential PM2.5 concentrations were estimated using a nationwide spatiotemporal model for women in the National Institutes of Health–AARP Diet and Health Study, a prospective cohort located in 6 states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and 2 metropolitan areas (Atlanta, GA, and Detroit, MI) and enrolled in 1995-1996 (n = 196 905). Annual average PM2.5 concentrations were estimated for a 5-year historical period 10 years prior to enrollment (1980-1984). We used Cox regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between a 10 µg/m3 increase in PM2.5 and breast cancer incidence overall and by estrogen receptor status and catchment area. Results With follow-up of participants through 2017, a total of 15 870 breast cancer cases were identified. A 10 ug/m3 increase in PM2.5 was statistically significantly associated with overall breast cancer incidence (HR = 1.08, 95% CI = 1.02 to 1.13). The association was evident for estrogen receptor–positive (HR = 1.10, 95% CI = 1.04 to 1.17) but not estrogen receptor–negative tumors (HR = 0.97, 95% CI = 0.84 to 1.13; Pheterogeneity = .3). Overall breast cancer hazard ratios were more than 1 across the catchment areas, ranging from a hazard ratio of 1.26 (95% CI = 0.96 to 1.64) for North Carolina to a hazard ratio of 1.04 (95% CI = 0.68 to 1.57) for Louisiana (Pheterogeneity = .9). Conclusions In this large US cohort with historical air pollutant exposure estimates, PM2.5 was associated with risk of estrogen receptor–positive breast cancer. State-specific estimates were imprecise but suggest that future work should consider region-specific associations and the potential contribution of PM2.5 chemical constituency in modifying the observed association.
Derivation and Internal Validation of a<scp>Disease‐Specific</scp>Cardiovascular Risk Prediction Model for Patients With Psoriatic Arthritis and Psoriasis
Authors: Keith Colaco, Ker‐Ai Lee, Shadi Akhtari, Raz Winer, Vinod Chandran, Paula Harvey, Richard J. Cook, Vincent Piguet, Dafna D. Gladman, Lihi Eder
Journal: Arthritis & Rheumatology (2023)

Objective To address suboptimal cardiovascular risk prediction in patients with psoriatic disease (PsD), we developed and internally validated a five‐year disease‐specific cardiovascular risk prediction model. Methods We analyzed data from a prospective cohort of participants with PsD without a history of cardiovascular events. Traditional cardiovascular risk factors and PsD‐related measures of disease activity were considered as potential predictors. The study outcome included nonfatal and fatal cardiovascular events. A base prediction model included 10 traditional cardiovascular risk factors. Eight PsD‐related factors were assessed by adding them to the base model to create expanded models, which were controlled for PsD therapies. Variable selection was performed using Least Absolute Shrinkage and Selection Operator (LASSO) penalized regression with 10‐fold cross‐validation. Model performance was assessed using measures of discrimination and calibration and measures of sensitivity and specificity. Results Between 1992 and 2020, 85 of 1,336 participants developed cardiovascular events. Discrimination of the base model (with traditional cardiovascular risk factors alone) was excellent, with an area under the receiver operator characteristic curve (AUC) of 85.5 (95% confidence interval [CI] 81.9–89.1). Optimal models did not select any of the tested disease‐specific factors. In a sensitivity analysis, which excluded lipid lowering and antihypertensive treatments, the number of damaged joints was selected in the expanded model. However, this model did not improve risk discrimination compared to the base model (AUC 85.5, 95% CI 82.0–89.1). Conclusion Traditional cardiovascular risk factors alone are effective in predicting cardiovascular risk in patients with PsD. A risk score based on these factors performed well, indicating excellent discrimination and calibration. image
Bioengineering Approaches for the Pancreatic Tumor Organoids Research and Application
Authors: Taiyu Song, Bin Kong, Rui Liu, Yuan Luo, Yongan Wang, Yuanjin Zhao
Journal: Advanced Healthcare Materials (2023)

Abstract Pancreatic cancer is a highly lethal form of digestive malignancy that poses significant health risks to individuals worldwide. Chemotherapy‐based comprehensive treatment is the primary therapeutic approach for midlife and late‐life patients. Nevertheless, the heterogeneity of the tumor and individual genetic backgrounds result in substantial variations in drug sensitivity among patients, rendering a single treatment regimen unsuitable for all patients. Conventional pancreatic cancer tumor organoid models are capable of emulating the biological traits of pancreatic cancer and are utilized in drug development and screening. However, these tumor organoids can still not mimic the tumor microenvironment (TME) in vivo, and the poor controllability in the preparation process hinders translation from essential drug screening to clinical pharmacological therapy. In recent years, many engineering methods with remarkable results have been used to develop pancreatic cancer organoid models, including bio‐hydrogel, co‐culture, microfluidic, and gene editing. Here, this work summarizes and analyzes the recent developments in engineering pancreatic tumor organoid models. In addition, the future direction of improving engineered pancreatic cancer organoids is discussed for their application prospects in clinical treatment.
Decoding the Association Between Body Composition in Preterm Birth and Hypertension in Childhood—Reply
Authors: James T. Nugent, Mona Sharifi, Jason H. Greenberg
Journal: JAMA Pediatrics (2023)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Journals JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Oncogenic KRASG12D Reprograms Lipid Metabolism by Upregulating SLC25A1 to Drive Pancreatic Tumorigenesis
Authors: Ruowen Zhang, Xiaogang Peng, James Xianxing Du, Rebecca Boohaker, Igor L. Estevao, Brian I. Grajeda, Marc B. Cox, Igor C. Almeida, Weiqin Lu
Journal: Cancer Research (2023)

Pancreatic cancer is a highly lethal disease with obesity as one of the risk factors. Oncogenic KRAS mutations are prevalent in pancreatic cancer and can rewire lipid metabolism by altering fatty acid (FA) uptake, FA oxidation (FAO), and lipogenesis. Identification of the underlying mechanisms could lead to improved therapeutic strategies for treating KRAS-mutant pancreatic cancer. Here, we observed that KRASG12D upregulated the expression of SLC25A1, a citrate transporter that is a key metabolic switch to mediate FAO, fatty acid synthesis, glycolysis, and gluconeogenesis. In genetically engineered mouse models and human pancreatic cancer cells, KRASG12D induced SLC25A1 upregulation via GLI1, which directly stimulated SLC25A1 transcription by binding its promoter. The enhanced expression of SLC25A1 increased levels of cytosolic citrate, FAs, and key enzymes in lipid metabolism. In addition, a high-fat diet (HFD) further stimulated the KRASG12D-GLI1-SLC25A1 axis and the associated increase in citrate and FAs. Pharmacologic inhibition of SLC25A1 and upstream GLI1 significantly suppressed pancreatic tumorigenesis in KrasG12D/+ mice on a HFD. These results reveal a KRASG12D-GLI1-SLC25A1 regulatory axis, with SLC25A1 as an important node that regulates lipid metabolism during pancreatic tumorigenesis, thus indicating an intervention strategy for oncogenic KRAS-driven pancreatic cancer.
Addressing genetic essentialism: Sharpening context in behavior genetics
Authors: Brian Byrne, Richard K. Olson
Journal: Behavioral and Brain Sciences (2023)

Abstract Evidence of a causal role for genes in human behavior underpins genetic essentialism, the scientifically flawed and socially hazardous idea that heritable characteristics are immutable. Behavior geneticists can challenge this idea by designing research that brings the contextual dependence of heritability estimates into sharper focus, and by incorporating a relevant statement into research reports and public outreach.
Extensions of the causal framework to Mendelian randomisation and gene–environment interaction
Authors: Claire M A Haworth, Robyn E Wootton
Journal: Behavioral and Brain Sciences (2023)

Abstract In our commentary we ask whether we should ultimately endeavour to find the deep causes of behaviours? Then we discuss two extensions of the proposed framework: (1) Mendelian randomisation and (2) hypothesis-free gene–environment interaction (leveraging heterogeneity in genetic associations). These complementary methods help move us towards second-generation causal knowledge, ultimately understanding mechanistic pathways and identifying more effective intervention targets.
Genomics might not be the solution, but epistemic validity remains a challenge in the social sciences
Authors: David Moreau, Kristina Wiebels
Journal: Behavioral and Brain Sciences (2023)

Abstract We sympathize with many of the points Burt makes in challenging the value of genetics to advance our understanding of social science. Here, we discuss how recent reflections on epistemic validity in the behavioral sciences can further contribute to a reappraisal of the role of sociogenomics to explain and predict human traits, aptitudes, and achievement.
When local causes are more explanatorily useful
Authors: Pierrick Bourrat
Journal: Behavioral and Brain Sciences (2023)

Abstract Madole &amp; Harden plead for better integration of causal knowledge of different depths to understand complex human traits. Classically, local causes – a particular type of shallow causes – are considered less useful than more generalisable causes, giving a false impression that the latter causes are more useful and desirable. Using a simple example, I show that sometimes the contrary is true.
Personalized lifetime prediction of survival and treatment benefit in patients with heart failure with reduced ejection fraction: The <scp>LIFE‐HF</scp> model
Authors: Pascal M. Burger, Gianluigi Savarese, Jasper Tromp, Carly Adamson, Pardeep S. Jhund, Lina Benson, Camilla Hage, Wan Ting Tay, Scott D. Solomon, Milton Packer, Xavier Rossello, John W. McEvoy, Dirk De Bacquer, Adam Timmis, Panos Vardas, Ian M. Graham, Emanuele Di Angelantonio, Frank L.J. Visseren, John J.V. McMurray, Carolyn S.P. Lam, Lars H. Lund, Stefan Koudstaal, Jannick A.N. Dorresteijn, Arend Mosterd
Journal: European Journal of Heart Failure (2023)